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Parkinson’s disease (PD) is the second most common neurodegenerative disease in the elder population, pathologically characterized by the progressive loss of dopaminergic neurons in the substantia nigra. While the precise mechanisms underlying the pathogenesis of PD remain unknown, various genetic factors have been proved to be associated with PD. To date, at least 23 loci and 19 disease-causing genes for PD have been identified. Although monogenic (often familial) cases account for less than 5% of all PD patients, exploring the phenotypes of monogenic PD can help us understand the disease pathogenesis and progression. Primary motor symptoms are important for PD diagnosis but only detectable at a relatively late stage. Despite typical motor symptoms, various non-motor symptoms (NMS) including sensory complaints, mental disorders, autonomic dysfunction, and sleep disturbances also have negative impacts on the quality of life in PD patients and pose major challenges for disease management. NMS is common in all stages of the PD course. NMS can occur long before the onset of PD motor symptoms or can present in the middle or late stage of the disease accompanied by motor symptoms. Therefore, the profiling and characterization of NMS in monogenic PD may help the diagnosis and differential diagnosis of PD, which thereby can execute early intervention to delay the disease progression. In this review, we summarize the characteristics, clinical phenotypes, especially the NMS of monogenic PD patients carrying mutations of SNCA, LRRK2, VPS35, Parkin, PINK1, DJ-1, and GBA. The clinical implications of this linkage between NMS and PD-related genes are also discussed.In older adults with normal cognition, cognitive reserve (CR) is known to be associated with the neuropsychological profile. We investigated the association between comprehensive CR and detailed neuropsychological profile in the early stage of cognitive decline. Fifty-five participants with mild cognitive impairment or subjective cognitive decline completed the cognitive reserve index questionnaire (CRIq) that yielded total, education, working activity, and leisure time scores (CRI-Total, CRI-Education, CRI-Working activity, and CRI-Leisure time, respectively). Mini-mental state examination (MMSE) and detailed neuropsychological evaluation were performed. Psychiatric symptom scales were applied to measure depression, apathy, positive or negative affect, and quality of life. Correlation and linear regression analyses of the variables were performed. The effect of CR-Education, CRI-Working activity, and CRI-Leisure time on the composite cognitive score was determined using a multivariable regression model. We observed that for CRI-Total (B = 3.00, p = 0.005), CRI-Education (B = 3.39, p = 0.002), and CRI-Leisure time (B = 2.56, p = 0.015), CR correlated with MMSE scores, while only CRI-Leisure time associated with the naming ability (B = 2.20, p = 0.033) in the detailed neuropsychological test results of the participants. Multivariable regression model also indicated that among CRI subscores, CRI-Leisure time directly affects the composite cognitive score (β = 0.32, p = 0.011). We found that in the early stage of cognitive decline in older adults, comprehensive CR was associated with global cognition, and only leisure activity was identified to be associated with the detailed neuropsychological profile including naming ability. These results may imply the positive effect of leisure activity on cognitive function in the early stages of cognitive decline.Running exercise, one of the strategies to protect brain function, has positive effects on neurons and synapses in the cortex and hippocampus. However, white matter, as an important structure of the brain, is often overlooked, and the effects of long-term running exercise on white matter are unknown. Here, 14-month-old male Sprague-Dawley (SD) rats were divided into a middle-aged control group (18-month-old control group), an old control group (28-month-old control group), and a long-term runner group (28-month-old runner group). The rats in the runner group underwent a 14-month running exercise regime. Spatial learning ability was tested using the Morris water maze, and white matter volume, myelinated fiber parameters, total mature oligodendrocyte number, and white matter capillary parameters were investigated using stereological methods. The levels of growth factors related to nerve growth and vascular growth in peripheral blood and the level of neurite outgrowth inhibitor-A (Nogo-A) in white matter were measured using an enzyme-linked immunosorbent assay (ELISA). The present results indicated that long-term running exercise effectively delayed the age-related decline in spatial learning ability and the atrophy of white matter by protecting against age-related changes in myelinated fibers and oligodendrocytes in the white matter. Moreover, long-term running exercise prevented age-related changes in capillaries within white matter, which might be related to the protective effects of long-term exercise on aged white matter.

Lifestyle interventions are promising strategies to promote cognitive health in aging. Projecte Moviment examines if aerobic exercise (AE), computerized cognitive training (CCT), and their combination (COMB) improves cognition, psychological health, and physical status compared to a control group. We assessed the moderating role of age and sex and the mediating effects of cardiorespiratory fitness (CRF), physical activity (PA), and psychological health on intervention-related cognitive benefits.

This was a 12-week multi-domain, single-blind, proof-of-concept randomized controlled trial (RCT). 96 healthy adults aged 50-70 years were assigned to AE, CCT, COMB, and a wait-list control group. The per protocol sample, which completed the intervention with a level of adherence > 80%, consisted of 82 participants (62% female; age = 58.38 ± 5.47). We assessed cognition, psychological health, CRF, and energy expenditure in PA at baseline and after the intervention. Selleckchem SU1498 We regressed change in each outcome on the treediating role of change in S-PA in these benefits.

http://www.ClinicalTrials.gov, identifier NCT03123900.

http://www.ClinicalTrials.gov, identifier NCT03123900.